Abstract
Proper understanding of the mechanisms involved in heart rate turbulence (HRT) may offer anexplanation of why it is such a potent postinfarction risk stratifier. This article reviews the physiologicalbackground of ventriculophasic sinus arrhythmia—a phenomenon which shares some underlying physiologicalfeatures with HRT including cardiac autonomic regulation. It is now believed that HRT is principally triggeredby a transient loss of vagal efferent activity in response to the missed baroreflex afferent input due toventricular premature beat-induced haemodynamically inefficient ventricular contraction. Studies are summarizedwhich support more or less directly this hypothesis. The physiology of early acceleration and late decelerationof heart rate after a ventricular premature beat is discussed. Qualitatively different but otherwisequantitatively uniform postectopic dynamics of systolic blood pressure after ventricular premature beats isdemonstrated in subjects with normal and abnormal left ventricular function. It is concluded that the slope oflate deceleration of heart rate after ventricular premature beats can serve as a reasonable surrogate forbaroreflex sensitivity.
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Wichterle, D., Melenovsky, V. & Malik, M. Mechanisms Involved in Heart Rate Turbulence. Card Electrophysiol Rev 6, 262–266 (2002). https://doi.org/10.1023/A:1016385126668
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DOI: https://doi.org/10.1023/A:1016385126668